Human cytomegalovirus (CMV) is a ubiquitous agent in human populations. Infections are generally asymptomatic, but there can be serious medical sequelae in immunocompromised individuals and in congenitally infected newborns. In immunocompromised individuals, CMV infection can result in interstitial pneumonia, retinitis progressing to blindness and disseminated infection. Infections in newborns can be severely damaging, with multiple organ involvement including the central nervous system and may also result in auditory damage. The mechanisms of pathogenesis are not understood, although it is believed that host factors, such as cellular and/or humoral immune responses might be involved.
CMV infects between 50-100% of all individuals worldwide depending on age and socioeconomic status. CMV is naturally transmitted via saliva, urine or breast milk but can also be recovered from other body secretions. In addition, CMV can be transmitted transplacentally to the fetus, by geno-urinary contact during birth or intercourse, by blood transfusion (especially white cells) and bone marrow or organ transplant.
CMV is associated with a wide variety of disease syndromes both in the immunocompetent and in the immunocompromised host, although the latter are much more frequent and associated with significantly greater morbidity and mortality. Primary infection in the immunocompetent host usually goes unnoticed. However CMV is considered to be causing 10% of the mononucleosis syndrome in adolescents and young adults and is frequently associated with acute nonA-G hepatitis. Primary infection in pregnant women is associated with the transplacental transfer of CMV to the fetus.
CMV is a significant opportunistic pathogen responsible for serious clinical consequences in a variety of immunosuppressed patient groups such as neonate and infants, persons with AIDS and individuals undergoing immunosuppressive regimes for the purpose of organ or bone marrow transplantation. As is true for other human herpes viruses, CMV establishes a life-long latent infection with its human host and is ubiquitous in the population with high infectivity rate found in the United States.
Although latent infection by CMV is widespread and reactivation of latent virus after either immunosuppression or progressive immunodeficiency is the single most important contributor to emergence of CMV disease, the site(s) of viral latency remain poorly characterized.
CMV-specific diagnosis can be achieved by a variety of techniques directly detecting viral components or indirectly measuring changes in the host immune status. Reliable diagnostic approaches require sensitive and reproducible technology based upon well defined and highly CMV-specific reagents and a detailed understanding of the molecular processes underlying CMV-infection in the human host.
An UL73-encoded structural glycoprotein (gN) expressed on the cell surface of infected cells (S. Pignatelli, et al., Arch Virol. 2002, 147:1247-56). The protein is highly polymorphic in the N-terminus, but conserved in the C-terminus (S. Pignatelli, et al. J Gen Virol. 2003, 84:647-5).